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IL-10-Dependent Crosstalk between Murine Marginal Zone B Cells, Macrophages, and CD8?+ Dendritic Cells Promotes Listeria monocytogenes Infection.


ABSTRACT: Type 1 CD8?+ conventional dendritic cells (cDC1s) are required for CD8+ T cell priming but, paradoxically, promote splenic Listeria monocytogenes infection. Using mice with impaired cDC2 function, we ruled out a role for cDC2s in this process and instead discovered an interleukin-10 (IL-10)-dependent cellular crosstalk in the marginal zone (MZ) that promoted bacterial infection. Mice lacking the guanine nucleotide exchange factor DOCK8 or CD19 lost IL-10-producing MZ B cells and were resistant to Listeria. IL-10 increased intracellular Listeria in cDC1s indirectly by reducing inducible nitric oxide synthase expression early after infection and increasing intracellular Listeria in MZ metallophilic macrophages (MMMs). These MMMs trans-infected cDC1s, which, in turn, transported Listeria into the white pulp to prime CD8+ T cells. However, this also facilitated bacterial expansion. Therefore, IL-10-mediated crosstalk between B cells, macrophages, and cDC1s in the MZ promotes both Listeria infection and CD8+ T cell activation.

SUBMITTER: Liu D 

PROVIDER: S-EPMC6685086 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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IL-10-Dependent Crosstalk between Murine Marginal Zone B Cells, Macrophages, and CD8α<sup>+</sup> Dendritic Cells Promotes Listeria monocytogenes Infection.

Liu Dong D   Yin Xiangyun X   Olyha Sam J SJ   Nascimento Manuela Sales L MSL   Chen Pei P   White Theresa T   Gowthaman Uthaman U   Zhang Tingting T   Gertie Jake A JA   Zhang Biyan B   Xu Lan L   Yurieva Marina M   Devine Lesley L   Williams Adam A   Eisenbarth Stephanie C SC  

Immunity 20190620 1


Type 1 CD8α<sup>+</sup> conventional dendritic cells (cDC1s) are required for CD8<sup>+</sup> T cell priming but, paradoxically, promote splenic Listeria monocytogenes infection. Using mice with impaired cDC2 function, we ruled out a role for cDC2s in this process and instead discovered an interleukin-10 (IL-10)-dependent cellular crosstalk in the marginal zone (MZ) that promoted bacterial infection. Mice lacking the guanine nucleotide exchange factor DOCK8 or CD19 lost IL-10-producing MZ B cell  ...[more]

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